T3. HEAT EXPOSURE, PTSD SEVERITY, AND IMMUNE MARKERS IN TRAUMA-EXPOSED ADULTS

Background Climate-related heat exposure is increasingly recognised as a potential environmental stressor for mental health, but biological mechanisms linking heat to post-traumatic stress disorder (PTSD) remain unclear. Inflammation is one plausible pathway, particularly in trauma-exposed populations. We examined whether recent ambient heat exposure was associated with PTSD severity and diagnosis, and whether C-reative protein (a systemic inflammatory marker) or selected cytokines (IL-1β, IL-6, IFN-γ, and TNF-α) modified these associations. Methods Participants from the Shared Roots Study, a South African trauma-exposed cohort, were linked to area-level daily weather data from the South African Weather Service. The primary exposure was mean daily maximum temperature over the 30 days preceding clinical assessment. The primary outcome variable was PTSD severity, measured using the CAPS-5 total score; PTSD diagnosis was analysed as a secondary binary outcome. CRP (n = 583) and observed individual cytokine concentrations for IL-1β (n = 172), IL-6 (n = 242), IFN-γ (n = 211), and TNF-α (n = 315) were log2-transformed prior to analysis. Cytokine values identified as below the assay detection threshold were treated as missing prior to log2 transformation. We tested heat-to-PTSD, heat-to-biomarker, biomarker-to-PTSD, and heat-by-biomarker interaction models, applying false discovery rate correction for multiple testing. Results Higher 30-day mean maximum temperature was positively associated with CAPS-5 total score (p = 0.04), and heat exposure was associated with significantly lower concentrations of IL-1β (n = p < 0.001), IL-6 (p < 0.001), and TNF-α (p = 0.022). However, individual cytokine levels were not significantly associated with CAPS-5 severity scores or PTSD diagnosis after multiple-testing correction, and heat-by-cytokine interaction terms were not statistically significant. CRP levels were not associated with heat exposure, CAPS-5 total score, or PTSD diagnosis. Discussion Recent heat exposure was associated with increased PTSD severity and with a reduction in IL-1β, IL-6, and TNF-α concentrations. However, these inflammatory markers did not robustly modify the association between heat exposure and PTSD outcomes, suggesting that, whilst marker-specific cytokine responses may reflect heat-related immune modulation, these do not robustly explain or amplify PTSD severity. Heat-related PTSD vulnerability may therefore involve non-inflammatory or more complex stress-biological mechanisms.

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Journal
European Neuropsychopharmacology
Published
2026-09-21
DOI
https://doi.org/10.1016/j.euroneuro.2026.113260
Primary Topic
Climate Change and Health Impacts
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article
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article

T3. HEAT EXPOSURE, PTSD SEVERITY, AND IMMUNE MARKERS IN TRAUMA-EXPOSED ADULTS

Soraya Seedat, Tahira Kootbodien, Setshaba Taukobong, Elisabeth Kathleen Webb et al.
European Neuropsychopharmacology
Climate Change and Health Impacts
article

T3. HEAT EXPOSURE, PTSD SEVERITY, AND IMMUNE MARKERS IN TRAUMA-EXPOSED ADULTS

Soraya Seedat, Tahira Kootbodien, Setshaba Taukobong, Elisabeth Kathleen Webb, Sian Megan Joanna Hemmings, Caradee Wright, Busi Shezi, Musa Aminu, Isaac Khobo, Matsepo Ramaboli
article en

Abstract

Background Climate-related heat exposure is increasingly recognised as a potential environmental stressor for mental health, but biological mechanisms linking heat to post-traumatic stress disorder (PTSD) remain unclear. Inflammation is one plausible pathway, particularly in trauma-exposed populations. We examined whether recent ambient heat exposure was associated with PTSD severity and diagnosis, and whether C-reative protein (a systemic inflammatory marker) or selected cytokines (IL-1β, IL-6, IFN-γ, and TNF-α) modified these associations. Methods Participants from the Shared Roots Study, a South African trauma-exposed cohort, were linked to area-level daily weather data from the South African Weather Service. The primary exposure was mean daily maximum temperature over the 30 days preceding clinical assessment. The primary outcome variable was PTSD severity, measured using the CAPS-5 total score; PTSD diagnosis was analysed as a secondary binary outcome. CRP (n = 583) and observed individual cytokine concentrations for IL-1β (n = 172), IL-6 (n = 242), IFN-γ (n = 211), and TNF-α (n = 315) were log2-transformed prior to analysis. Cytokine values identified as below the assay detection threshold were treated as missing prior to log2 transformation. We tested heat-to-PTSD, heat-to-biomarker, biomarker-to-PTSD, and heat-by-biomarker interaction models, applying false discovery rate correction for multiple testing. Results Higher 30-day mean maximum temperature was positively associated with CAPS-5 total score (p = 0.04), and heat exposure was associated with significantly lower concentrations of IL-1β (n = p < 0.001), IL-6 (p < 0.001), and TNF-α (p = 0.022). However, individual cytokine levels were not significantly associated with CAPS-5 severity scores or PTSD diagnosis after multiple-testing correction, and heat-by-cytokine interaction terms were not statistically significant. CRP levels were not associated with heat exposure, CAPS-5 total score, or PTSD diagnosis. Discussion Recent heat exposure was associated with increased PTSD severity and with a reduction in IL-1β, IL-6, and TNF-α concentrations. However, these inflammatory markers did not robustly modify the association between heat exposure and PTSD outcomes, suggesting that, whilst marker-specific cytokine responses may reflect heat-related immune modulation, these do not robustly explain or amplify PTSD severity. Heat-related PTSD vulnerability may therefore involve non-inflammatory or more complex stress-biological mechanisms.

European NeuropsychopharmacologyVol. 111
South African Medical Research Council (ZA), Duke University (US), Stellenbosch University (ZA), Nelson Mandela University (ZA)
Climate action
Openalex Percentile: Top 11%
Climate Change and Health Impacts
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